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Alam, Muhammad S; Otsuka, Shizuka; Wong, Nathan; Abbasi, Aamna; Gaida, Matthias M; Fan, Yu; Meerzaman, Daoud; Ashwell, Jonathan D
Proceedings of the National Academy of Sciences - PNAS, 12/2021, Letnik: 118, Številka: 50Journal Article
TNF, produced largely by T and innate immune cells, is potently proinflammatory, as are cytokines such as IFN-γ and IL-17 produced by Th1 and Th17 cells, respectively. Here, we asked if TNF is upstream of Th skewing toward inflammatory phenotypes. Exposure of mouse CD4 T cells to TNF and TGF-β generated Th17 cells that express low levels of IL-17 (ROR-γt IL-17 ) and high levels of inflammatory markers independently of IL-6 and STAT3. This was mediated by the nondeath TNF receptor TNFR2, which also contributed to the generation of inflammatory Th1 cells. Single-cell RNA sequencing of central nervous system-infiltrating CD4 T cells in mouse experimental autoimmune encephalomyelitis (EAE) found an inflammatory gene expression profile similar to cerebrospinal fluid-infiltrating CD4 T cells from patients with multiple sclerosis. Notably, TNFR2-deficient CD4 T cells produced fewer inflammatory mediators and were less pathogenic in EAE and colitis. IL-1β, a Th17-skewing cytokine, induced TNF and proinflammatory granulocyte-macrophage colony-stimulating factor (GM-CSF) in T cells, which was inhibited by disruption of TNFR2 signaling, demonstrating IL-1β can function indirectly via the production of TNF. Thus, TNF is not just an effector but also an initiator of inflammatory Th differentiation.
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